1. Field of the Invention
This invention relates generally to the treatment of a group of physiological disorders known as complex regional pain syndrome, which is a multi-system, multi-symptom, syndrome usually affecting one or more extremities (but can affect any other part of the body) by the electrical stimulation of the corresponding cluster of nerves and/or ganglia in the sympathetic chain, adjacent to the corresponding vertebrae.
2. Description of the Prior Art
Within the field of neurosurgery, the use of electrical stimulation for the treatment of pathologies, including such disorders as uncontrolled movement, such as Parkinson""s disease and essential tremor, as well as chronic pain and eating disorders, has been widely discussed in the literature. It has been recognized that electrical stimulation holds significant advantages over alternative methods of treatment, for example lesioning, inasmuch as successful lesioning destroys all nerve activity. Collateral damage to non-targeted tissues is also a significant risk in lesioning treatments. In many instances, it is, therefore, the preferred effect is to stimulate or reversibly block nervous tissue. Electrical stimulation permits such stimulation of the target neural structures, and equally importantly, it does not require the destruction of the nervous tissue (it is a reversible process, which can literally be shut off or removed at will). In addition, stimulation parameters can be adjusted so that benefits are maximized, and side effects are minimized.
The particular application which the present invention is directed to, is the treatment of complex regional pain syndromes. Complex regional pain syndrome (CRPS) type I, commonly known as reflex sympathetic dystrophy syndrome, or RSDS, was described 25 years ago. Several synonyms have been commonly employed in describing parts or all of this syndrome, including Raynaud""s syndrome, vasomotor instability, occupational digital thrombosis, arteriosclerotic obliterative disease, etc. CPRS Type II, on the other hand, also known as causalgia, is a regional pain syndrome that develops after injury to a peripheral nerve, as first described during the Civil War by Dr. W. Mitchell. Spontaneous pain develops in the territory of the affected nerve which may then spread beyond that region. Vasomotor abnormalities and focal edema may occur alone or in combination in both CRPS types I and II. These are a severely disabling group of illness with simultaneous involvement of nerve, skin, muscle, blood vessels, and bones. While there are many symptoms associated with CRPS, the only common denominator is pain. The pain usually appears in one or more extremities, and is described as chronic, burning, and constant in nature. A syndrome of total body pain due to CRPS has been described as well. The remainder of symptoms may or may not occur. These symptoms include swelling, limited motor function which may lead to atrophy or dystrophy, tremor, focal dystonia or spasm, skin changes such as atrophy, dryness, and scaling, as well as bony changes with joint tenderness and swelling. In addition, vasomotor instability consisting of Raynaud""s phenomenon (e.g. color changes and pain in fingers when exposed to cold), vasoconstriction or dilatation leading to cold and warm extremities respectively, as well as increased sweating.
The cause of the condition is currently not well understood and is often unrecognized. A number of precipitating factors have been associated with CRPS including minor trauma, cerebral or spinal cord lesions, ischemic heart disease and/or myocardial infarction, and repetitive cumulative trauma, such as carpal tunnel syndrome. However, in many of the patients a definite precipitating event can not be identified. Duration of CRPS varies, in many cases the pain continues on for at least two years and in some cases, indefinitely. Some patients experience periods of remissions and exacerbations. Periods of remission may last for weeks, months or years. The mean age of onset is in the mid thirties and there is increasing evidence that the incidence of CRPS in adolescents and young adults is on the rise. In Germany alone, for example, the annual incidence of RSD is estimated at 15000 [Dertwinkel, 1998]. Both sexes are affected, but the incidence of the syndrome is higher in women. Nonsurgical treatment consists of medicinal therapy, physical therapy, various peripheral or sympathetic nerve blocks, transcutaneous electrical nerve stimulation, or surgical sympathectomy. Patient response to therapy directly correlates to early diagnosis and treatment. However, the overall response rate to treatment is poor with over 50% of patients having significant pain and/or disability years later.
Abnormalities of autonomic function are present in both CRPS types I and II. Autonomic dysfunction results in localized sweating and changes in blood flow that may result in temperature asymmetries between affected and unaffected limbs. The changes in blood flow and sweating may result from localized noradrenergic and cholinergic hypersensitivity. Each body area has a regional cluster of nerve cells extending along the outside of the spinal column, and forming the sympathetic nervous system.
For example, the sympathetic outflow to the upper extremity lies in the inferior portion of the stellate or cervicothoracic ganglion down to the third thoracic ganglion. Similarly for the lower extremity, the sympathetic outflow passes through the second through fourth sympathetic ganglia. In general terms, the sympathetic, along with the parasympathetic, nervous system is part of the autonomic, or vegetative, nervous system. The effects of the autonomic system are extensive, and range from the control of blood pressure, heart rate, sweat, and body heat, to blood glucose levels, sexual arousal, and digestion.
While there are a variety of different techniques and mechanisms which have been designed to focus the lesioning means directly onto the target nerve tissue, collateral damage is inevitable. Were it even possible to direct all lesioning energy onto the target nerve cluster, it is a significant drawback that other functioning of these nerves is lost, even when such functioning may not be pathological. In addition, there are several common side effects described in the medical literature, including an ipsilateral Horner""s syndrome (drooping eyelid and smaller pupil), compensatory sweating (increased sweating in other areas), and gustatory sweating (sweating, particularly of the face, at the smell of certain foods). It is because of the development of these and other side effects, including the poor response of medical or surgical therapy especially after a delay in treatment, that thoracic or lumbar sympathectomy has not enjoyed a greater popularity among physicians.
These complications, however, can be minimized to a large extent, or possible eliminated, by the use of chronic electrical stimulation or continuous drug infusion. The reasons are many, and include the possibility of changing which contacts of a multipolar lead are stimulated to minimize stimulating the superior portion of the stellate ganglion which can lead to a Horner""s syndrome, to adjusting the parameters such as frequency or pulse width to affect changes in compensatory and gustatory sweating, should they arise. In addition, parameters may be intermittently adjusted if, and when, clinical efficacy is worsening in order to maximize therapeutic benefit
It is therefore the principle object of the present invention to provide a less destructive and fully reversible and adjustable method of treating complex regional pain syndromes by electrically or chemically stimulating/inhibiting the appropriate portion(s) of the sympathetic chain.
The preceding objects are provided in the present invention, which comprises new and novel methods of treating complex regional pain syndromes by implantation of stimulation electrodes at specific locations along the sympathetic chain. More particularly the present invention comprises a method of therapeutically treating upper or lower extremity CRPS Type I or II by surgically implanting an electrode adjacent to a predetermined site along the sympathetic chain on the affected side of the body, or if clinically indicated, bilaterally. For upper extremity reflex sympathetic dystrophy (CRPS Type I), for example, this involves the surgical implantation of a stimulating electrode over the inferior portion of the stellate ganglion, and over T2-4. The most commonly employed surgical approach is aided by video-assisted thoracoscopy, which involves the placement of 2-4 small incisions or ports in the chest wall, through which instruments may traverse en route to the lateral aspect of the vertebral bodies where the sympathic chain lies extrapleurally. The distal end of the lead can be secured to surrounding tissues and be placed either directly over the sympathetic chain or over the internal aspect of the parietal pleura. The proximal end of the lead can be passed out of the thoracic cavity via one of the neighboring surgical ports, and tunneled subcutaneously to an electrical signal source which, in turn, is operated to stimulate the predetermined treatment site over the sympathetic ganglia, such that the clinical effects of the pain disorder are reduced with minimal side effects.
Alternatively, a catheter with either end- or side-apertures placed over the ganglia of interest is connected in a similar fashion to a infusion pump. In addition, this embodiment is extended to include a combination electrical contact and drug delivery system, as well as a system which has the capacity to sense or record electrical or chemical activity in the region of interest.